RANTES, MIP and interleukin-16 in HIV infection

Blazevic, Vesna; Heino, Maarit; Ranki, Annamari; Jussila, T.; Krohn, Kai

doi:10.1097/00002030-199610000-00021

Cited by 21 publications

(11 citation statements)

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“…3), and the level of production was not dependent on an individual's absolute count or percentage of peripheral blood CD4ϩ cells, we conclude that there is no correlation between clinical state and chemokine production by PBMC, CD4ϩ, or CD8ϩ T cells. Other investigators in more limited studies have reached a similar conclusion in studies of CD8ϩ cells (44,46) as well as all three of these cell populations (47). The elevated ␤-chemokine production in AIDS patients would suggest that these chemokines are not protecting against disease progression either by their ability to competitively inhibit HIV interaction with its coreceptor on CD4ϩ cells, or by a protective mechanism based on their chemotactic activities.…”

Section: Discussionsupporting

confidence: 66%

Do beta-chemokines have clinical relevance in HIV infection?

Mackewicz

Barker²,

Greco³

et al. 1997

J. Clin. Invest.

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The role of ␤ -chemokines in HIV infection was evaluated. The kinetics of regulated upon activation of normal T cell expressed and secreted, macrophage inflammatory protein-1 ␣ , and macrophage inflammatory protein 1 ␤ production by stimulated T lymphocytes did not differ substantially between HIV-infected (asymptomatic and with AIDS) and uninfected subjects. Maximal production of these ␤ -chemokines by activated peripheral blood cells was higher in the infected individuals than in uninfected individuals, but no significant difference was observed between healthy infected subjects and AIDS patients. Evaluation of the effect of HIV replication on ␤ -chemokine production indicated that acute infection of CD4 ϩ T cells with non-syncytia-inducing (NSI) viruses generally increased ␤ -chemokine production two to eightfold, whereas with SI strains, it led to decreased production. The sensitivity of an individual's virus to ␤ -chemokine-mediated inhibition correlated with the NSI virus phenotype and a healthy clinical state. 50% of the AIDS patients, however, had NSI viruses that were sensitive to ␤ -chemokines. Finally, anti-␤ -chemokine-neutralizing antibodies caused a more rapid release of HIV by CD4 ϩ T cells naturally infected by NSI, but not SI, viruses indicating that endogenously produced chemokines can affect HIV production in culture. These findings suggest that ␤ -chemokines may affect HIV replication when an NSI virus is involved, but provide little evidence that they substantially influence HIV infection and pathogenesis. ( J. Clin. Invest. 1997. 100: 921-930.)

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Section: Discussionsupporting

confidence: 66%

Do beta-chemokines have clinical relevance in HIV infection?

Mackewicz

Barker²,

Greco³

et al. 1997

J. Clin. Invest.

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“…Moreover, recent results indicate that human alloimmunization elicits very significant increases in the three ␤ chemokines RANTES, MIP-1␣, and MIP-1␤, and resistance of CD4 ϩ T cells to HIV infection with macrophagetropic HIV-1 strains (38). However, when the production of ␤ chemokines by unfractionated PBMCs, purified CD4 ϩ , or CD8 ϩ T cells was examined in small numbers of HIV-1 positive subjects, the analysis failed to demonstrate any association between chemokine levels and disease stage (39,40). Furthermore, plasma levels of ␤ chemokines did not reveal any substantial differences between progressors and nonprogressors (41)(42)(43)(44)(45)(46).…”

mentioning

confidence: 99%

Higher macrophage inflammatory protein (MIP)-1α and MIP-1β levels from CD8⁺T cells are associated with asymptomatic HIV-1 infection

Cocchi

DeVico

Yarchoan

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

129

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To test the hypothesis that ␤-chemokine levels may be relevant to the control of HIV in vivo, we compared RANTES, MIP-1␣, and MIP-1␤ production from purified CD8 ؉ T cells from 81 HIV-infected subjects and from 28 uninfected donors. Asymptomatic HIV ؉ subjects produced significantly higher levels of MIP-1␣ and MIP-1␤, but not RANTES, than uninfected donors or patients that progressed to AIDS. In contrast, ␤ chemokines in plasma were either nondetectable or showed no correlation with clinical status. The high ␤-chemokine-mediated anti-HIV activity was against the macrophage tropic isolate HIV-1BAL, with no demonstrable effect on the replication of the T-cell tropic HIV-1 IIIB. These findings suggest that constitutive ␤-chemokine production may play an important role in the outcome of HIV-1 infection.

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“…Although the bchemokines can effectively block HIV replication in vitro and CCR5 seems to have a clear role in HIV pathogenesis, there has been no consistent difference observed between chemokine levels from nonprogressing HIV-infected persons, progressing HIV-infected persons, and HIV-uninfecte d persons. [2][3][4][5][6] This has created controversy about the in vivo role of these chem okines in the pathogenesis of HIV disease. One explanation for these differing results may be due to the measurement of chem okines under different experim ental conditions.…”

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confidence: 99%

Sustained Suppression of Plasma HIV RNA Is Associated with an Increase in the Production of Mitogen-Induced MIP-1alpha and MIP-1beta

Kumar

Parato²,

Kumar³

et al. 1999

AIDS Research and Human Retroviruses

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The chemokine receptor CCR5 has been shown to be a major coreceptor for HIV-1. The chemokines that bind to this receptor (MIP-1alpha, MIP-1beta, and RANTES) are potent inhibitors of HIV replication and may play an important role in the pathophysiology of HIV disease. We investigated the effect of potent antiretroviral therapy (ritonavir and saquinavir) on the production of MIP-1alpha, MIP-1beta, and RANTES in 19 HIV-infected patients who had sustained decreases in plasma HIV RNA levels (<200 copies/ml). Chemokine concentrations were measured in serum, plasma, and PHA-stimulated PBMCs at baseline and 24 and 48 weeks after initiating therapy. MIP-1alpha, MIP-1beta, and RANTES levels in serum and plasma did not significantly change in the 48-week period. In contrast, MIP-1alpha and MIP-1beta secreted by PHA-stimulated PBMCs increased at 24 weeks, with this increase sustained at 48 weeks, whereas no significant change was observed in PHA-induced RANTES production. A significant positive correlation was found between the changes in PHA-induced chemokine production and baseline CD4+ T cell counts. These data demonstrate that sustained suppression of viral replication by potent antiretroviral therapy has a potentially beneficial effect on chemokine production and early initiation of this therapy appears to confer a more favorable chemokine profile.

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RANTES, MIP and interleukin-16 in HIV infection

Cited by 21 publications

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Do beta-chemokines have clinical relevance in HIV infection?

Do beta-chemokines have clinical relevance in HIV infection?

Higher macrophage inflammatory protein (MIP)-1α and MIP-1β levels from CD8⁺T cells are associated with asymptomatic HIV-1 infection

Sustained Suppression of Plasma HIV RNA Is Associated with an Increase in the Production of Mitogen-Induced MIP-1alpha and MIP-1beta

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RANTES, MIP and interleukin-16 in HIV infection

Cited by 21 publications

References 0 publications

Do beta-chemokines have clinical relevance in HIV infection?

Do beta-chemokines have clinical relevance in HIV infection?

Higher macrophage inflammatory protein (MIP)-1α and MIP-1β levels from CD8+T cells are associated with asymptomatic HIV-1 infection

Sustained Suppression of Plasma HIV RNA Is Associated with an Increase in the Production of Mitogen-Induced MIP-1alpha and MIP-1beta

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Higher macrophage inflammatory protein (MIP)-1α and MIP-1β levels from CD8⁺T cells are associated with asymptomatic HIV-1 infection